A high-fat diet can cause Intestinal Cancer, study finds

“Nature” is an international journal of Science. It has published a study which says that a diet constituting a high content of fats can be a potential cause of cancer. A high-fat diet can make the cellular linings of your intestine prone to cancer. The results of the study suggested that obesity, high-fat or a high-calorie diet can serve as potential factors for various kinds of cancers.

The paper discussing the study is entitled as “High-fat diet enhances stemness and tumorigenicity of intestinal progenitors.” It illustrates how a high-fat diet affects the structure and function of the intestine in mammals. The study specifically focuses on the intestinal stem cells and non-intestinal stem cells and their capacity to create and initiate tumors.

The stem cells last a lifetime. They live in intestine linings known as the epithelium. They, in turn, create all of the different cell types that compose the epithelium.

The co-lead author of the study, Semir Beyaz says that high-fat content drives a pool of intestinal stem cells and other cells that behave like stem cells. These cells then, reproduce themselves indefinitely and differentiate into other cell types. According to him, the behavior exhibited by these cells is what brings about intestinal tumors.

David Sabatini, M.D., Ph.D. of the Whitehead Institute and Yilmaz, an assistant professor of biology and member of Massachusetts Institute of Technology‘s (MIT) Koch Institute for Integrative Cancer Research served as co-authors of the study. In addition, Miyeko Mana, MIT post-doctoral student and Jatin Roper, MIT visiting scientist, were the lead authors.

The experiments for the study employed a population of mice. They were fed with a diet consisting of 60 percent fat for a period of nine months to a year. The study verified the correlation between stem cells and cancer linked to obesity.

The researchers of the study found that mice fed with high-fat diet acquired 50 percent more body mass and developed more intestinal tumors. On the other side, mice fed normally exhibited no such symptoms.

The leading supporters of the study were,

Howard Hughes Medical Institute

Ellison Medical Foundation

National Institutes of Health, Department of Defense,

Center for the Study of Inflammatory Bowel Diseases at Massachusetts General Hospital

Kathy and Curt Marble Cancer Research Fund

American Federation of Aging Research

V Foundation for Cancer Research.

The researchers isolated the intestinal cells from the mice and grew them in a culture dish. The researchers discovered that cells from mice under the high-fat diet brought about “mini-intestines.” Moreover, they also identified that mice under the high-fat diet produced progenitor cells. Progenitor cells are differentiated daughter cells of the stem cells. They exhibited behavior similar to stem cells like they had an extended lifespan and ability to generate mini-intestines outside of its body.

In addition, the researchers also revealed the presence of a hyper-activated nutrient-sensing pathway. The pathway is known as the fatty acid sensor PPAR-delta. It enables a metabolic process to convert fats, instead of carbohydrates and sugars, to energy. PPAR-delta is also found to activate a gene set essential to stem cell identity.

Beyaz further extended his explanation. He said that the epidemiological link between a high-fat diet and colorectal cancer has been reported for many years. However, the underlying mechanisms were not known. This study, for the first time, enumerated a compact mechanism of,

How a high-fat diet regulates intestinal stem cell function?

How this regulation contributes to tumor formation?

Future studies are being carried out to target narrowing down possible cancer drugs that will address tumors due to obesity. This respective study also supports previous researches which claim that obese people are more likely to have colorectal cancer. It also indicated that intestinal stem cells are the most likely to acquire mutations resulting to colon cancer.